AQA biology unit 5

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  • Created by: Saf
  • Created on: 20-06-11 22:07

Basics & Negative feedback

  • External environment changes effect the internal environment.
  • Keeping your internal environment constant is vital to stop cells from malfunctioning/being damaged, and homestasis does just this.
  • Especially important to maintain temperature (too high & enzymes can become denatured, too low & the enzyme activity is reduced-optimum 37'C) and pH (too high/low then enzymes are denatured- optimum is pH7)
  • Glucose concentration is also an important factor to maintain. Too high- water potential reduced so H2O molecules diffuse by osmosis out of cells into blood (cells shrivel up & die) Too low- cells stop working as there's not enough glucose to provide energy.

Negative feedback:

  • Receptors detect when a level is too high/low, info is sent via nervous/hormonal system to the effectors, which counteract the change.
  • This is negative feedback, which brings all the levels back to normal.
  • Multiple feedback systems mean a faster return to normal, as it actively increases/decreases a level e.g. in a car, take foot off accelerator slows you down, but using the brake aswell would slow you down a lot faster.
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Positive feedback

Positive Feedback:

  • Amplifies any change to levels.
  • Positive feedback makes the levels which have changed fluctuate further away from the norm.
  • Useful to quickly activate something e.g. blood clot
  • Not involved in homeostasis as it doesn't keep environment constant.


  • Low body temperature (below 35'C)
  • Result of heat being lost from the body faster than it's being produced.
  • Brain stops working properly, shivering stops making body even colder.
  • Positive feedback makes body temperature drop even further (going away from the norm temperature) unless help is found.
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Control of body temperature

Ectotherms (e.g. reptiles/fish):

  • Can't control temperature internally, change behaviour instead-go in sun etc
  • Internal temperature depends on their external surroundings.
  • More active at higher temperatures & less active at low temperatures.
  • Variable metabolic rate, don't generate a lot of heat themselves.

Endotherms (e.g. mammals/birds):

  • Control body temperature internally & by behaviour (by finding shade etc).
  • Internal temperature less affected by external temperature (up to a point).
  • Can be active at any external temperature (up to a point).
  • high metabolic rate & generate a lot of heat from metabolic reactions.
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Mammalian methods of controlling body temperature

Heat Loss:

  • Sweating- secreted from sweat glands, then evaporates, cooling skin.
  • Hairs lie flat- erector pili muscles relax, less air is trapped- more heat lost.
  • Vasodilation- arterioles near surface dilate and more blood flows through capillaries, so more heat is lost by radiation.

Heat Production:

  • Shivering- muscles contract in spasms, more heat is produced (increased rate of respiration).
  • Hormones- adreneline released- increases metabolic rate- more heat.

Heat Conservation:

  • Less sweat- reduced amount of heat loss.
  • Hairs stand up-erector pili muscles contract, hairs trap air& insulate body.
  • Vasoconstriction- arterioles constrict, less blood flows, reduces heat loss.
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Hypothalamus' role in controlling body temperature

  • Part of the brain (the hypothalmus) maintains a constant body temperature.
  • Gets info about both internal & external temperature from thermoreceptors.
  • Internal temperature info is from thermoreceptors in hypothalmus which detect blood temperature.
  • External temperature info is from thermoreceptors in skin which detect skin temperature.
  • Thermoreceptors send impulses along sensory neurones to hypothalmus, which sends impulses along motor neurones to effectors (muscles/glands).
  • All unconcious- via the autonomic nervous system.
  • Effectors use methods shown on the previous card ("mammalian methods...") to return temperature to normal (i.e. 37'C).
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Controlling blood glucose concentration

  • Cells in pancreas monitor blood glucose concentration (BGC)
  • BGC rises after eating carbohydrates (get energy from these) and falls after exercise (more glucose is used in respiration to produce energy).
  • Controlled by the hormones insulin & glucagon (negative feedback)
  • Beta cells secrete insulin & alpha cells secrete glucagon.

Insulin Lowers BGC when it's too high...

  • Binds to receptors in liver & muscle cells and increases the permeability to glucose, so cells take up more glucose.
  • Also activates enzymes which convert glucose into glycogen (glycogenesis).
  • Increases rate of respiration of glucose, esp. in muscle cells.

Glucagon raises BGC when it's too low...

  • Binds to specific receptors in liver cells, activates enzymes which convert glycogen into glucose (glycogenolysis) and also converts amino acids into glucose (gluconeogenesis)
  • Glucagon decreases rate of respiration of glucose in cells.
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  • Hormone which is secreted from adrenal glands (above your kidneys) when there's a low blood glucose concentration (BCG)
  • Binds to receptors in liver cell membranes
  • Activates glycogenolysis (glycogen --> glucose)
  • Inhibits glycogenesis (glucose --> glycogen)
  • Inhibits insulin secretion & activates glucagon secretion.
  • Body is ready for action as it has more glucose available for muscles to use in respiration.

Can also activate glycogenolysis inside a cell...

  • Adrenaline& glucagon bind to receptors- activate adenylate cyclase enzyme.
  • Enzyme converts ATP into a chemical messenger ("second messenger").
  • Second messenger called cyclic AMP (cAMP).
  • cAMP activates chain of reactions: glycogen --> glucose (glycogenolysis)
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Diabetes is when blood glucose concentration can't be controlled properly...

Type 1:

  • Beta cells (in islets of langerhans) don't produce any insulin
  • After eating, BGC levels rise&stay high-hyperglycaemia- can end in death.
  • Kidneys can't reabsorb extra glucose, so some of it is excreted in urine.
  • Injections help treat this, but too many and hypoglycaemia can occur (dramatic drop in BGC levels). Eating regularly & less sugar also helps.

Type 2:

  • Usually aquired later in life- linked to obesity.
  • Beta cells don't produce enough insulin/ body cells dont respond properly to insulin (e.g. their insulin receptors on membranes don't work.)
  • Results in cells not taking up enough glucose, so BGC levels are high.
  • Treated by losing weight and controlling amount of sugars eaten.
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Menstrual Cycle

  • Follicle develops in the ovary.
  • Ovulation- egg is released.
  • Uterus lining thickens so fertilised egg can implant.
  • Corpus luteum (corp lut.) develops from follicle remains.
  • No fertilisation- lining breaks down & leaves body (menstruation).


  • Follicle-stimulating hormone (FSH)- stimulates follicle to develop.
  • Luteinising hormone (LH)- stimulates ovulation & development of corp lut.
  • Oestrogen (O)- stimulates thickening of uterus
  • Progesterone (P)- maintains thick uterus lining
  • FSH & LH secreted by anterior pituitary gland. O & P secreted by ovaries.
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Menstrual Cycle 2

  • High FHS- follicle develops- releases O. FSH stimulates ovaries to release O
  • O conc. rises- stimulates lining to thicken. Inhibits FSH being released.
  • O conc. peaks- stimulates pituitary gland to release LH and FSH.
  • Surge of LH- stimulates ovulation. Corp lut. develops & releases P.
  • P conc. rises- inhibits FSH & LH release. Lining maintained. No fertilisation- corp lut. breaks down & stops releasing P.
  • P conc. falls- FSH & LH conc. increase (no longer inhibited by P). Lining isn't maintained, so it breaks down & leaves body (menstruation).

Negative Feedback:

  • FSH stimulates release of O. O inhibits release of FSH.- no more follicles!
  • LH stimulates corp. lut to develop producing P, P inhibits release of LH- no more follicles develop & lining broken down if no fertilisation occurs.

Positive feedback:

  • O stimulates release of LH, which stimulates release of more O etc etc.
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